Biomedical Sciences ETDs

Publication Date

Fall 12-13-2025

Abstract

Orthohantaviruses are zoonotic, negative-sense RNA viruses maintained in persistently infected rodent reservoirs, where they cause no disease yet drive severe vascular pathology in humans. This dissertation investigates how Seoul orthohantavirus (SEOV) establishes persistence within reservoir endothelial cells while avoiding antiviral signaling that would otherwise restrict replication. Comparative infections in rat and human endothelial cells show that SEOV genomic RNAs form perinuclear microdomains in reservoir cells but remain dispersed in human cells. These virus-induced structures colocalize with the Golgi, ERGIC, ER, and mitochondria, revealing striking host-specific membrane remodeling. This remodeling reflects a fundamental divergence in SEOV’s replication strategy across host species and may underlie its evasion of the cytosolic RNA sensor RIG-I without direct antagonism. Together, these findings identify organelle remodeling as a structural mechanism supporting immune evasion and persistence in the natural host, illuminating broader principles of viral persistence, immune modulation, and hantavirus–reservoir coevolution.

Keywords

Orthohantavirus, Innate Immunity, Endothelial Cells, RIG-I-like Receptors, Viral Immune Evasion, Reservoir Host Tolerance

Document Type

Dissertation

Language

English

Degree Name

Biomedical Sciences

Level of Degree

Doctoral

Department Name

Biomedical Sciences Graduate Program

First Committee Member (Chair)

Judy Cannon

Second Committee Member

Alison M Kell

Third Committee Member

Michelle Ozbun

Fourth Committee Member

William Curt Hines

Fifth Committee Member

Michael Mandell

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Available for download on Monday, December 13, 2027

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